Vestibular neuritis is one of the most common causes of vertigo. The etiology is unknown, though it is widely assumed to be a viral illness. This project intends to investigate the role of herpes simplex virus (HSV) and varicella zoster virus (VZV) in the pathogenesis of vestibular neuritis. These viruses are selected for study for several reasons. First, they are known to establish latent infection in the vestibular ganglion. Second, reactivation of latent herpes virus can result in acute dysfunction of a cranial nerve as is seen in acute facial paralysis in Bell's palsy (HSV) and Ramsay Hunt syndrome (VZV). Third, vestibular symptoms occur in conjunction with acute facial palsy in a minority of cases. Finally, inoculation of animals with HSV can produce acute vestibular dysfunction. Some surgeons remove the vestibular ganglion when performing vestibular neurectomy to treat patients with chronic vertigo. Excised surgical specimens from patients with the pre-operative diagnosis of vestibular neuritis, Meniere's disease and other miscellaneous chronic vestibulopathies will be analyzed for the presence of herpes virus DNA using contemporary molecular diagnostic techniques. The prevalence of each virus in the ganglion will be compared with the prevalence in a randomly selected group of cadavers. A significant increase in the prevalence of one or both viruses in the vestibular neuritis group would constitute a firm epidemiological link between the virus and the disease. The sub-aims of the project will attempt to quantify the number of ganglion cells harboring latent virus and the number of copies of the viral genome per ganglion in the study and control groups. Experimental evidence suggests the potential for reactivation is proportional to the percentage of ganglion cells infected and the viral load per cell. This information can help determine why some individuals with latent virus in the vestibular ganglion develop clinical symptoms due to reactivation and some do not.